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. Author manuscript; available in PMC: 2010 Apr 12.
Published in final edited form as: Future Med Chem. 2009 Apr;1(1):95–118. doi: 10.4155/fmc.09.6

Table 3.

Trisaccharides.

graphic file with name nihms-133110-f0005.jpg

Study Compound Assays* Activity Lit. no. Ref.
Jaworek (2001) IG-29 Lipogenesis Inactive 1 [72]
Dietrich (1999) Conformational study 4 [39]

Jaworek (2001) IG-30 Lipogenesis Inactive 2 [72]
Frick (1998) IG-31 Lipogenesis Inactive 1 [45]
Frick (1999) 15% MIR EC50 = 25 μM H [101]
Glucose transport 2% MIR, EC50 = 10 μM

Frick (1998) IG-32 Lipogenesis 20% MIR at 100 μM 7 [45]
Frick (1999) 25% MIR, EC50 = 15 μM G [101]
Frick (1998) Glucose transport 40% MIR at 20 μM 7 [45]
Frick (1999) 9% MIR, EC50 = 15 μM G [101]
Frick (1998) GPAT 25% MIR 7 [45]
Glycogenesis 33% MIR at 20 μM
GLUT4 translocation 50% MIR
Lipolysis 42% MIR
Tyrosine phosphorylation of IRS-1 30% MIR at 10 μM

Frick (1998) IG-33 Lipogenesis Activity ‘B’* 8 [45]

McLean (2008) IG-34 PDH phosphatase Negligible activity for PDP activation 15 [32]
PDK inhibition 0.2% inhibition of PDK at 1 mM
*

Details of assays (in alphabetical order) are given in the text.

The number assigned to this compound in the cited publication.

§

Note: For Muller’s SAR study [45] aggregate activities were reported as follows: “A”, MIR < 20%; “B”, MIR 20–49%, EC20 25–200 μM; “C”, MIR 50–80%, EC50 10–100 μM; “D”, MIR > 80%, EC50 3–30 μM.

Lit. no.: Literacy number; MIR: Maximal insulin response; PDH: Pyruvate dehydrogenase; PDK: Phosphoinositide-dependent kinase.